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Pediatrics > Hemolytic and Haemorrhagic diseases of newborn > Flashcards

Hemolytic and Haemorrhagic diseases of newborn Flashcards

1
Q

Newborns predisposition to vit. K deficiency

A
  • this coagulation abnormality leads to serious bleeding
  • transplacental trasfer of vitamin K is very limited during pregnancy
  • storage of vit. K in liver is also very limited in newborns
  • once the infantile gut is colonized with bacterial flora, microbial production of vit. K results in lower riks of bleeding related to deficiency
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2
Q

Vitamin K deficiency in breast fed infants

A
  • breast milk is a poor source of vitamin K (1-4µg/l)
  • recommended dietary intake is 1 µg/l/day
  • exclusively breastfed infants have intestinal colonization with lactobacilli that do not produce vit. K
  • reduced production of menaquinone (vit K2) increases neonatal risk of bleeding
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3
Q

Vitamin K dependent proteins

A
  • Factor II (prothrombin)
  • Factor VII (Proconvertin)
  • Factor IX (Thromboplastin component)
  • Factor X (Stuart factor)
  • Protein C and S
  • Protein Z
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4
Q

Vitamin K effect on clotting cascade

A

If not enough vitmain K present –> cltting factors are not synthesized enough –> clotting cascade is not functioning

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5
Q

Clotting cascade intrinsic pathway

A

Damaged Surface –> kininogen, Kallikrein

  • -> XII –> XIIa
  • -> XI –> XIa
  • -> IX –> IXa
  • -> VIIIa helpts X turn to Xa
  • -> Xa activates Va
  • -> Va turns protrombin to thrombin
  • -> thrombin turns fibrinogen to fibrin
  • -> with XIIIa cross-linked fibrin clot produced
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6
Q

Clotting cascade extrinsic pathway

A

Traume

  • -> VII –> VIIa
  • -> VIIa acitvated tissue factor
  • -> tissue factor turns X to Xa
  • -> Xa activates Va
  • -> Va turns protrombin to thrombin
  • -> thrombin turns fibrinogen to fibrin
  • -> with XIIIa cross-linked fibrin clot produced
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7
Q

Primary hemolytic disease of newborn (HDN)

A
  • often fatal
  • diffuse hemorrhage in otherwise healthy infant
  • in first week of life
  • mostly in low weight babies
  • low levels of prothrombin and other vit K dependent clotting factors
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8
Q

Clinical Manifestation of pirmary HDN

A

bleeding in

  • GI
  • Urinary tract
  • umbilical stump
  • nose
  • scalp
  • intracranial
  • injection sites
  • shock
  • death
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9
Q

Prophylactic use of vitamin K

A
  • intramuscular administration within the first 6 hours after birth are effective in preventing both early and late HDN
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10
Q

Treatment of vitamin K deficiency

A
  • vit K1 (phytonadione) for prothrombin, proconvertin and thromboplastin component and stuart factor
  • coagulation factors should increase in 6-12 hours after PO dosing and 1-2 hours after parenteral
  • for life threatening hemorrhages along with IV administration of Vitamin K, 10-20ml per kg body weigzht fresh frozen plasma should be adminstered
  • if blood loss > 20% and there is evidence of shock: immediate blood transfusion
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11
Q

Definition of Hemolytic disease of newborn (HDN)

A

Condition in which fetus or neonate’s red blood cells are destroyed by IgG antibodies produced by mother

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12
Q

Rh hemolytic disease of the newborn

A
  • mother is Rh negative
  • Rh sensitization is not likely in first pregnancy
  • in next pregnancy: mother’s antibodies cross the placenta then reacts with an RBC antigen to fight the Rh positive cells in the baby’s body
  • antigen-antibody interaction occurs
  • sensitization of baby’s RBC by mother’s IgG antibody causes baby’s RBC to be destroyed
  • Ab coated RBCs are removed from fetal corculation by the macrphages of the spleen and liver
  • anemia willstimulate bone marrow t produce immature RBC –> erythroblastosis fetalis
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13
Q

Clinical features of Rh hemolytic disease of the newborn

A

LESS SEVERE
- mild anemia

SEVERE
- icterus gravis neonatorum (Kernicterus)

INTRAUTERINE DEATH
- hyrops fetalis –> edematous, ascites, bulky swollen and friable placenta because extravascular hamolysis with extramedullary eryhthorpoiesis and hepatic and cardiac failure

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14
Q

Kramer’s rule

A

Evaluation of the degree of jaundice in newborn

1st zone: yello head, neck, sclera
2nd zone: yellow trunk
3rd zone: hypogastric region
4th zone: extremities
5th zone: all the body, severe
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15
Q

Prevention of Rh hemolytic disease of the newborn

A
  • all non.sensitized Rh D-negative women should be given anti-d immunoglobulin at 28 adn 34 weeks of gestation
  • at birth, if baby is Rh- –> no further treatment
  • if baby is Rh+ –> porphylactic anti-D should be administered within 72h of delivery
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16
Q

Treatment of Rh hemolytic disease of the newborn

A

UNBORN BABY
- intrauterine blood transfusion

NEWBORN BABY

  • phototherapy
  • exchange transfusion
  • intravenous immunoglobulun (IVIG) to prevent destruction of RBC
17
Q

Intrauterine blood transfusion

A
  • to replace fetal RBCs that are being detroyed by the Rh sensitized mother’s immune system
  • is meant to keep fetus healthy until it is mature enough the be delivered
  • in severely affected fetus: tranfusions every 1-4 weeks
18
Q

Management of indirect hyperbilirubinemia

A
  • visual assessment
  • blood level monitoring at 24 h of life or sooner
  • interpretation of risk levels and need for treatment
  • -> phototherapy
  • -> exchange transfusions
  • -> IVIG
  • -> Phenobarbital
19
Q

Transcutaneous bilirubinometry

A
  • measures the bilirubin level by contact with skin

- does not reflect exact bilirubin levels but gives a general idea about bilirubin levels in the blood

20
Q

Bhutani Curve

A

If the baby is in the range of the curve, phototherapy should start

The earlier the hyperbilirubinemia starts, phototherapy should also start

21
Q

Important factors in efficacy of phototherapy

A
  • distance
  • skin area exposed
  • irradiance
  • spectrum of light
22
Q

Exchange blood transfusion

A
  • removes sensitized cells
  • reduces level of meternal antibody
  • removes about 60% of plasma bilirubin, resulting in clearnace of about 30-40% of total bilirubin
  • corrects anemia
  • replacement with donor plasma restores albumin and any needed coagulation factors
  • usually two volume exchanges are needded as bilirubin from tissues will return to the blood stream
  • first blood is taken from the baby, then transufison the blood (25 procedures)
23
Q

Clinical outcomes of hyperbilirubinemia

A
  • Deposits in skin and mucous membranes –> jaundice
  • Unconjucated bilirubin deposits in the brain –> acute bilirubin encephalopathy
  • Permanent neuronal damage –> kernicterus
24
Q

ABO incompatibility

A
  • most common cause of HDN
  • with blood types A and B, isoimmunization does not occur because the naturally occurring antibodies are IgM, not IgG
  • in type O mothers: antibodies are predominantly IgG, cross the placenta and can cause hemolysis in fetus
  • HDN only occurs in 3%
  • ABO can occur in first pregnancies
  • clinical presentation usually less severe than with Rh disease
25
Q

Diagnosis and treatment of ABO imcompatibility

A
  • diagnosis and investigation are the same as Rh disease
  • Treatment is by phototherapy and exchange transfusion
  • no effective prevention against ABO incompatibility reaction
26
Q

Differential diagnosis

A
  • hemorrhage in the newborn
  • failure of erythrocyte production in newborn
  • conjugated hyperbilirubinemia

Pediatrics (11 decks)

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